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10.3109/08977194.2011.595714

http://scihub22266oqcxt.onion/10.3109/08977194.2011.595714
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suck abstract from ncbi


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pmid21740331
      Growth+Factors 2011 ; 29 (5 ): 196-202
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  • TGF-? signaling in fibrosis #MMPMID21740331
  • Biernacka A ; Dobaczewski M ; Frangogiannis NG
  • Growth Factors 2011[Oct]; 29 (5 ): 196-202 PMID21740331 show ga
  • Transforming growth factor ? (TGF-?) is a central mediator of fibrogenesis. TGF-? is upregulated and activated in fibrotic diseases and modulates fibroblast phenotype and function, inducing myofibroblast transdifferentiation while promoting matrix preservation. Studies in a wide range of experimental models have demonstrated the involvement of the canonical activin receptor-like kinase 5/Smad3 pathway in fibrosis. Smad-independent pathways may regulate Smad activation and, under certain conditions, may directly transduce fibrogenic signals. The profibrotic actions of TGF-? are mediated, at least in part, through induction of its downstream effector, connective tissue growth factor. In light of its essential role in the pathogenesis of fibrosis, TGF-? has emerged as an attractive therapeutic target. However, the pleiotropic and multifunctional effects of TGF-? and its role in tissue homeostasis, immunity and cell proliferation raise concerns regarding potential side effects that may be caused by TGF-? blockade. This minireview summarizes the role of TGF-? signaling pathways in the fibrotic response.
  • |Animals [MESH]
  • |Cell Differentiation [MESH]
  • |Cell Proliferation [MESH]
  • |Connective Tissue Growth Factor/metabolism [MESH]
  • |Extracellular Matrix/*pathology [MESH]
  • |Fibroblasts/metabolism [MESH]
  • |Fibrosis/*metabolism/pathology/physiopathology [MESH]
  • |Humans [MESH]
  • |Mice [MESH]
  • |Mitogen-Activated Protein Kinases/metabolism [MESH]
  • |Signal Transduction [MESH]
  • |Smad Proteins/metabolism [MESH]


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